Biomarkers of vascular disease in diabetes: the adipose-immune system cross talk

Andrea Flex, Federico Biscetti, Elisabetta Nardella, Andrea Leonardo Cecchini, Raffaele Landolfi

Risultato della ricerca: Contributo in rivistaArticolo in rivista

4 Citazioni (Scopus)

Abstract

Experimental and clinical studies aimed at investigating the mechanism(s) underlying vascular complications of diabetes indicate that a great number of molecules are involved in the pathogenesis of these complications. Most of these molecules are inflammatory mediators or markers generated by immune or adipose tissue. Some of them, i.e. resistin and sortilin, have been shown to be involved in the cross talk between adipocytes and inflammatory cells. This interaction is an attractive area of research, particularly in type 2 diabetes and obesity. Other proteins, such as adiponectin and visfatin, appear to be more promising as possible vascular markers. In addition, some molecules involved in calcium/phosphorus metabolism, such as klotho and FGF23, have an involvement in the pathogenesis of diabetic vasculopathy, which appears to be dependent on the degree of vascular impairment. Inflammatory markers are a promising tool for treatment decisions while measuring plasma levels of adipokines, sortilin, Klotho and FGF23 in adequately sized longitudinal studies is expected to allow a more precise characterization of diabetic vascular disease and the optimal use of personalized treatment strategies.
Lingua originaleEnglish
pagine (da-a)381-393
Numero di pagine13
RivistaInternal and Emergency Medicine
Volume15
DOI
Stato di pubblicazionePubblicato - 2020

Keywords

  • Atherosclerosis
  • Tumor Necrosis Factor-alpha
  • Diabetes
  • Vascular complications
  • Adaptor Proteins, Vesicular Transport
  • Adipokines
  • Adipose Tissue
  • Biomarkers
  • C-Reactive Protein
  • Cardiovascular Diseases
  • Diabetes Mellitus, Type 2
  • Exosomes
  • Glucuronidase
  • HMGB Proteins
  • Humans
  • Immune System
  • Interleukin-1
  • Osteoprotegerin
  • Prevalence
  • Serum Amyloid P-Component
  • Signal Transduction

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